Effect of a transitory ischaemia on the structure-linked latency of rat liver acid phosphatase and beta-galactosidase.
The structure-linked latency of acid phosphatase and beta-galactosidase was studied in rat liver lobes made ischaemic for 1 or 2 h and then recirculated with blood for increasing periods. Free activity of acid phosphatase and unsedimentable activity of beta-galactosidase are increased in homogenates of ischaemic livers. When ischaemia had been maintained for 1 h, the recovery of normal latency for both enzymes was observed 1 h after re-establishment of the blood flow. After a 2 h period of ischaemia, unmasked activity markedly decreases during the first 1 h after restoration of blood flow; after that, a large and irreversible secondary rise takes place. Chlorpromazine, injected 30 min before or just after induction of ischaemia, extensively prevents the latency decrease occurring during restoration of blood flow. Modifications of the hydrolase distribution pattern obtained after differential centrifugation are in agreement with the latency changes. These results suggest that a 2 h ischaemia causes an alteration of the liver lysosomes that is largely reversible and that restoration of blood flow induces an irreversible alteration of these organelles. Chlorpromazine treatment prevents the irreversible lesion from taking place.
D000135:Acid Phosphatase / Q000097:blood / Q000378:metabolism*; D000818:Animals; D002498:Centrifugation; D002746:Chlorpromazine / Q000494:pharmacology; D005696:Galactosidases / Q000378:metabolism*; D007511:Ischemia / Q000201:enzymology*; D008099:Liver / Q000098:blood supply / Q000187:drug effects / Q000201:enzymology*; D008297:Male; D051381:Rats; D001616:beta-Galactosidase / Q000097:blood / Q000378:metabolism*
D000135:Acid Phosphatase; D005696:Galactosidases; D001616:beta-Galactosidase; D002746:Chlorpromazine